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1. Genome-wide association study identifies multiple susceptibility loci for pancreatic cancer

Author

Wolpin, Brian M, Rizzato, Cosmeri, Kraft, Peter, Kooperberg, Charles, Petersen, Gloria M, Wang, Zhaoming, Arslan, Alan A, Beane-Freeman, Laura, Bracci, Paige M, Buring, Julie, Canzian, Federico, Duell, Eric J, Gallinger, Steven, Giles, Graham G, Goodman, Gary E, Goodman, Phyllis J, Jacobs, Eric J, Kamineni, Aruna, Klein, Alison P, Kolonel, Laurence N, Kulke, Matthew H, Li, Donghui, Malats, Núria, Olson, Sara H, Risch, Harvey A, Sesso, Howard D, Visvanathan, Kala, White, Emily, Zheng, Wei, Abnet, Christian C, Albanes, Demetrius, Andreotti, Gabriella, Austin, Melissa A, Barfield, Richard, Basso, Daniela, Berndt, Sonja I, Boutron-Ruault, Marie-Christine, Brotzman, Michelle, Büchler, Markus W, Bueno-de-Mesquita, H Bas, Bugert, Peter, Burdette, Laurie, Campa, Daniele, Caporaso, Neil E, Capurso, Gabriele, Chung, Charles, Cotterchio, Michelle, Costello, Eithne, Elena, Joanne, Funel, Niccola, Gaziano, J Michael, Giese, Nathalia A, Giovannucci, Edward L, Goggins, Michael, Gorman, Megan J, Gross, Myron, Haiman, Christopher A, Hassan, Manal, Helzlsouer, Kathy J, Henderson, Brian E, Holly, Elizabeth A, Hu, Nan, Hunter, David J, Innocenti, Federico, Jenab, Mazda, Kaaks, Rudolf, Key, Timothy J, Khaw, Kay-Tee, Klein, Eric A, Kogevinas, Manolis, Krogh, Vittorio, Kupcinskas, Juozas, Kurtz, Robert C, LaCroix, Andrea, Landi, Maria T, Landi, Stefano, Le Marchand, Loic, Mambrini, Andrea, Mannisto, Satu, Milne, Roger L, Nakamura, Yusuke, Oberg, Ann L, Owzar, Kouros, Patel, Alpa V, Peeters, Petra HM, Peters, Ulrike, Pezzilli, Raffaele, Piepoli, Ada, Porta, Miquel, Real, Francisco X, Riboli, Elio, Rothman, Nathaniel, Scarpa, Aldo, Shu, Xiao-Ou, Silverman, Debra T, Soucek, Pavel, Sund, Malin, Talar-Wojnarowska, Renata, Taylor, Philip R, and Theodoropoulos, George E

Subjects
Cancer, Aged, Case-Control Studies, Female, Genetic Loci, Genetic Predisposition to Disease, Genome-Wide Association Study, Genotype, Humans, Male, Middle Aged, Pancreatic Neoplasms, Polymorphism, Single Nucleotide, White People, Biological Sciences, Medical and Health Sciences, Developmental Biology
Abstract

We performed a multistage genome-wide association study including 7,683 individuals with pancreatic cancer and 14,397 controls of European descent. Four new loci reached genome-wide significance: rs6971499 at 7q32.3 (LINC-PINT, per-allele odds ratio (OR) = 0.79, 95% confidence interval (CI) 0.74-0.84, P = 3.0 × 10(-12)), rs7190458 at 16q23.1 (BCAR1/CTRB1/CTRB2, OR = 1.46, 95% CI 1.30-1.65, P = 1.1 × 10(-10)), rs9581943 at 13q12.2 (PDX1, OR = 1.15, 95% CI 1.10-1.20, P = 2.4 × 10(-9)) and rs16986825 at 22q12.1 (ZNRF3, OR = 1.18, 95% CI 1.12-1.25, P = 1.2 × 10(-8)). We identified an independent signal in exon 2 of TERT at the established region 5p15.33 (rs2736098, OR = 0.80, 95% CI 0.76-0.85, P = 9.8 × 10(-14)). We also identified a locus at 8q24.21 (rs1561927, P = 1.3 × 10(-7)) that approached genome-wide significance located 455 kb telomeric of PVT1. Our study identified multiple new susceptibility alleles for pancreatic cancer that are worthy of follow-up studies.

Published
2014

2. Family history of cancer and risk of pancreatic cancer: a pooled analysis from the Pancreatic Cancer Cohort Consortium (PanScan).

Author

Jacobs, Eric J, Chanock, Stephen J, Fuchs, Charles S, Lacroix, Andrea, McWilliams, Robert R, Steplowski, Emily, Stolzenberg-Solomon, Rachael Z, Arslan, Alan A, Bueno-de-Mesquita, H Bas, Gross, Myron, Helzlsouer, Kathy, Petersen, Gloria, Zheng, Wei, Agalliu, Ilir, Allen, Naomi E, Amundadottir, Laufey, Boutron-Ruault, Marie-Christine, Buring, Julie E, Canzian, Federico, Clipp, Sandra, Dorronsoro, Miren, Gaziano, J Michael, Giovannucci, Edward L, Hankinson, Susan E, Hartge, Patricia, Hoover, Robert N, Hunter, David J, Jacobs, Kevin B, Jenab, Mazda, Kraft, Peter, Kooperberg, Charles, Lynch, Shannon M, Sund, Malin, Mendelsohn, Julie B, Mouw, Tracy, Newton, Christina C, Overvad, Kim, Palli, Domenico, Peeters, Petra HM, Rajkovic, Aleksandar, Shu, Xiao-Ou, Thomas, Gilles, Tobias, Geoffrey S, Trichopoulos, Dimitrios, Virtamo, Jarmo, Wactawski-Wende, Jean, Wolpin, Brian M, Yu, Kai, and Zeleniuch-Jacquotte, Anne

Subjects
Humans, Pancreatic Neoplasms, Genetic Predisposition to Disease, Case-Control Studies, Cohort Studies, Genome-Wide Association Study, Colo-Rectal Cancer, Clinical Research, Rare Diseases, Aging, Cancer, Digestive Diseases, Prostate Cancer, Ovarian Cancer, Pancreatic Cancer, Breast Cancer, Prevention, Urologic Diseases, 2.1 Biological and endogenous factors, Oncology & Carcinogenesis, Oncology and Carcinogenesis
Abstract

A family history of pancreatic cancer has consistently been associated with increased risk of pancreatic cancer. However, uncertainty remains about the strength of this association. Results from previous studies suggest a family history of select cancers (i.e., ovarian, breast and colorectal) could also be associated, although not as strongly, with increased risk of pancreatic cancer. We examined the association between a family history of 5 types of cancer (pancreas, prostate, ovarian, breast and colorectal) and risk of pancreatic cancer using data from a collaborative nested case-control study conducted by the Pancreatic Cancer Cohort Consortium. Cases and controls were from cohort studies from the United States, Europe and China, and a case-control study from the Mayo Clinic. Analyses of family history of pancreatic cancer included 1,183 cases and 1,205 controls. A family history of pancreatic cancer in a parent, sibling or child was associated with increased risk of pancreatic cancer [multivariate-adjusted odds ratios (ORs) = 1.76, 95% confidence interval (CI) = 1.19-2.61]. A family history of prostate cancer was also associated with increased risk (OR = 1.45, 95% CI = 1.12-1.89). There were no statistically significant associations with a family history of ovarian cancer (OR = 0.82, 95% CI = 0.52-1.31), breast cancer (OR = 1.21, 95% CI = 0.97-1.51) or colorectal cancer (OR = 1.17, 95% CI = 0.93-1.47). Our results confirm a moderate sized association between a family history of pancreatic cancer and risk of pancreatic cancer and also provide evidence for an association with a family history of prostate cancer worth further study.

Published
2010

3. Alcohol intake and pancreatic cancer: a pooled analysis from the pancreatic cancer cohort consortium (PanScan)

Author

Michaud, Dominique S, Vrieling, Alina, Jiao, Li, Mendelsohn, Julie B, Steplowski, Emily, Lynch, Shannon M, Wactawski-Wende, Jean, Arslan, Alan A, Bas Bueno-de-Mesquita, H, Fuchs, Charles S, Gross, Myron, Helzlsouer, Kathy, Jacobs, Eric J, LaCroix, Andrea, Petersen, Gloria, Zheng, Wei, Allen, Naomi, Ammundadottir, Laufey, Bergmann, Manuela M, Boffetta, Paolo, Buring, Julie E, Canzian, Federico, Chanock, Stephen J, Clavel-Chapelon, Françoise, Clipp, Sandra, Freiberg, Matthew S, Michael Gaziano, J, Giovannucci, Edward L, Hankinson, Susan, Hartge, Patricia, Hoover, Robert N, Allan Hubbell, F, Hunter, David J, Hutchinson, Amy, Jacobs, Kevin, Kooperberg, Charles, Kraft, Peter, Manjer, Jonas, Navarro, Carmen, Peeters, Petra HM, Shu, Xiao-Ou, Stevens, Victoria, Thomas, Gilles, Tjønneland, Anne, Tobias, Geoffrey S, Trichopoulos, Dimitrios, Tumino, Rosario, Vineis, Paolo, Virtamo, Jarmo, Wallace, Robert, Wolpin, Brian M, Yu, Kai, Zeleniuch-Jacquotte, Anne, and Stolzenberg-Solomon, Rachael Z

Subjects
Health Services and Systems, Biomedical and Clinical Sciences, Health Sciences, Alcoholism, Alcohol Use and Health, Cancer, Digestive Diseases, Pancreatic Cancer, Rare Diseases, Clinical Research, Substance Misuse, Oral and gastrointestinal, Good Health and Well Being, Aged, Alcohol Drinking, Case-Control Studies, Cohort Studies, Female, Humans, Male, Pancreatic Neoplasms, Prospective Studies, Alcohol, Pancreatic cancer, Pooled analysis, Oncology and Carcinogenesis, Public Health and Health Services, Epidemiology, Oncology and carcinogenesis
Abstract

The literature has consistently reported no association between low to moderate alcohol consumption and pancreatic cancer; however, a few studies have shown that high levels of intake may increase risk. Most single studies have limited power to detect associations even in the highest alcohol intake categories or to examine associations by alcohol type. We analyzed these associations using 1,530 pancreatic cancer cases and 1,530 controls from the Pancreatic Cancer Cohort Consortium (PanScan) nested case-control study. Odds ratios (OR) and 95% confidence intervals (95% CI) were calculated using unconditional logistic regression, adjusting for potential confounders. We observed no significant overall association between total alcohol (ethanol) intake and pancreatic cancer risk (OR = 1.38, 95% CI = 0.86-2.23, for 60 or more g/day vs. >0 to

Published
2010

4. A genome-wide association study identifies pancreatic cancer susceptibility loci on chromosomes 13q22.1, 1q32.1 and 5p15.33.

Author

Petersen, Gloria M, Amundadottir, Laufey, Fuchs, Charles S, Kraft, Peter, Stolzenberg-Solomon, Rachael Z, Jacobs, Kevin B, Arslan, Alan A, Bueno-de-Mesquita, H Bas, Gallinger, Steven, Gross, Myron, Helzlsouer, Kathy, Holly, Elizabeth A, Jacobs, Eric J, Klein, Alison P, LaCroix, Andrea, Li, Donghui, Mandelson, Margaret T, Olson, Sara H, Risch, Harvey A, Zheng, Wei, Albanes, Demetrius, Bamlet, William R, Berg, Christine D, Boutron-Ruault, Marie-Christine, Buring, Julie E, Bracci, Paige M, Canzian, Federico, Clipp, Sandra, Cotterchio, Michelle, de Andrade, Mariza, Duell, Eric J, Gaziano, J Michael, Giovannucci, Edward L, Goggins, Michael, Hallmans, Göran, Hankinson, Susan E, Hassan, Manal, Howard, Barbara, Hunter, David J, Hutchinson, Amy, Jenab, Mazda, Kaaks, Rudolf, Kooperberg, Charles, Krogh, Vittorio, Kurtz, Robert C, Lynch, Shannon M, McWilliams, Robert R, Mendelsohn, Julie B, Michaud, Dominique S, Parikh, Hemang, Patel, Alpa V, Peeters, Petra HM, Rajkovic, Aleksandar, Riboli, Elio, Rodriguez, Laudina, Seminara, Daniela, Shu, Xiao-Ou, Thomas, Gilles, Tjønneland, Anne, Tobias, Geoffrey S, Trichopoulos, Dimitrios, Van Den Eeden, Stephen K, Virtamo, Jarmo, Wactawski-Wende, Jean, Wang, Zhaoming, Wolpin, Brian M, Yu, Herbert, Yu, Kai, Zeleniuch-Jacquotte, Anne, Fraumeni, Joseph F, Hoover, Robert N, Hartge, Patricia, and Chanock, Stephen J

Subjects
Chromosomes, Human, Pair 1, Chromosomes, Human, Pair 5, Chromosomes, Human, Pair 13, Humans, Carcinoma, Pancreatic Neoplasms, Genetic Predisposition to Disease, Case-Control Studies, Cohort Studies, Linkage Disequilibrium, Polymorphism, Single Nucleotide, Genome-Wide Association Study, Genetic Loci, Rare Diseases, Cancer, Genetics, Clinical Research, Pancreatic Cancer, Digestive Diseases, Human Genome, Biological Sciences, Medical and Health Sciences, Developmental Biology
Abstract

We conducted a genome-wide association study of pancreatic cancer in 3,851 affected individuals (cases) and 3,934 unaffected controls drawn from 12 prospective cohort studies and 8 case-control studies. Based on a logistic regression model for genotype trend effect that was adjusted for study, age, sex, self-described ancestry and five principal components, we identified eight SNPs that map to three loci on chromosomes 13q22.1, 1q32.1 and 5p15.33. Two correlated SNPs, rs9543325 (P = 3.27 x 10(-11), per-allele odds ratio (OR) 1.26, 95% CI 1.18-1.35) and rs9564966 (P = 5.86 x 10(-8), per-allele OR 1.21, 95% CI 1.13-1.30), map to a nongenic region on chromosome 13q22.1. Five SNPs on 1q32.1 map to NR5A2, and the strongest signal was at rs3790844 (P = 2.45 x 10(-10), per-allele OR 0.77, 95% CI 0.71-0.84). A single SNP, rs401681 (P = 3.66 x 10(-7), per-allele OR 1.19, 95% CI 1.11-1.27), maps to the CLPTM1L-TERT locus on 5p15.33, which is associated with multiple cancers. Our study has identified common susceptibility loci for pancreatic cancer that warrant follow-up studies.

Published
2010

5. Genome-wide association study identifies variants in the ABO locus associated with susceptibility to pancreatic cancer.

Author

Amundadottir, Laufey, Kraft, Peter, Stolzenberg-Solomon, Rachael Z, Fuchs, Charles S, Petersen, Gloria M, Arslan, Alan A, Bueno-de-Mesquita, H Bas, Gross, Myron, Helzlsouer, Kathy, Jacobs, Eric J, LaCroix, Andrea, Zheng, Wei, Albanes, Demetrius, Bamlet, William, Berg, Christine D, Berrino, Franco, Bingham, Sheila, Buring, Julie E, Bracci, Paige M, Canzian, Federico, Clavel-Chapelon, Françoise, Clipp, Sandra, Cotterchio, Michelle, de Andrade, Mariza, Duell, Eric J, Fox, John W, Gallinger, Steven, Gaziano, J Michael, Giovannucci, Edward L, Goggins, Michael, González, Carlos A, Hallmans, Göran, Hankinson, Susan E, Hassan, Manal, Holly, Elizabeth A, Hunter, David J, Hutchinson, Amy, Jackson, Rebecca, Jacobs, Kevin B, Jenab, Mazda, Kaaks, Rudolf, Klein, Alison P, Kooperberg, Charles, Kurtz, Robert C, Li, Donghui, Lynch, Shannon M, Mandelson, Margaret, McWilliams, Robert R, Mendelsohn, Julie B, Michaud, Dominique S, Olson, Sara H, Overvad, Kim, Patel, Alpa V, Peeters, Petra HM, Rajkovic, Aleksandar, Riboli, Elio, Risch, Harvey A, Shu, Xiao-Ou, Thomas, Gilles, Tobias, Geoffrey S, Trichopoulos, Dimitrios, Van Den Eeden, Stephen K, Virtamo, Jarmo, Wactawski-Wende, Jean, Wolpin, Brian M, Yu, Herbert, Yu, Kai, Zeleniuch-Jacquotte, Anne, Chanock, Stephen J, Hartge, Patricia, and Hoover, Robert N

Subjects
Chromosomes, Human, Pair 9, Humans, Pancreatic Neoplasms, Genetic Predisposition to Disease, ABO Blood-Group System, Logistic Models, Odds Ratio, Risk Factors, Case-Control Studies, Cohort Studies, Prospective Studies, Gene Frequency, Genotype, Haplotypes, Linkage Disequilibrium, Polymorphism, Single Nucleotide, Alleles, Introns, United States, Female, Male, Genetic Variation, Genome-Wide Association Study, Prevention, Rare Diseases, Cancer, Genetics, Clinical Research, Pancreatic Cancer, Digestive Diseases, Human Genome, 2.1 Biological and endogenous factors, Aetiology, Biological Sciences, Medical and Health Sciences, Developmental Biology
Abstract

We conducted a two-stage genome-wide association study of pancreatic cancer, a cancer with one of the lowest survival rates worldwide. We genotyped 558,542 SNPs in 1,896 individuals with pancreatic cancer and 1,939 controls drawn from 12 prospective cohorts plus one hospital-based case-control study. We conducted a combined analysis of these groups plus an additional 2,457 affected individuals and 2,654 controls from eight case-control studies, adjusting for study, sex, ancestry and five principal components. We identified an association between a locus on 9q34 and pancreatic cancer marked by the SNP rs505922 (combined P = 5.37 x 10(-8); multiplicative per-allele odds ratio 1.20; 95% confidence interval 1.12-1.28). This SNP maps to the first intron of the ABO blood group gene. Our results are consistent with earlier epidemiologic evidence suggesting that people with blood group O may have a lower risk of pancreatic cancer than those with groups A or B.

Published
2009

6. Receptor activator of nuclear factor kB ligand, osteoprotegerin, and risk of death following a breast cancer diagnosis: results from the EPIC cohort

Author

Sarink, Danja, Schock, Helena, Johnson, Theron, Chang-Claude, Jenny, Overvad, Kim, Olsen, Anja, Tjønneland, Anne, Arveux, Patrick, Fournier, Agnès, Kvaskoff, Marina, Boeing, Heiner, Karakatsani, Anna, Trichopoulou, Antonia, La Vecchia, Carlo, Masala, Giovanna, Agnoli, Claudia, Panico, Salvatore, Tumino, Rosario, Sacerdote, Carlotta, Van Gils, Carla H, Peeters, Petra HM, Weiderpass, Elisabete, Agudo, Antonio, Rodríguez-Barranco, Miguel, Huerta, José María, Ardanaz, Eva, Gil, Leire, Kaw, Kay Tee, Schmidt, Julie A, Dossus, Laure, His, Mathilde, Aune, Dagfinn, Riboli, Elio, Kaaks, Rudolf, and Fortner, Renée T

Subjects
musculoskeletal diseases, Adult, Risk, Epidemiology, RANK Ligand, Osteoprotegerin, Breast Neoplasms, Middle Aged, Prognosis, 3. Good health, Cohort Studies, Breast cancer, Limit of Detection, Case-Control Studies, Humans, Female, Reproductive, hormonal, and related factors, Serum biomarkers of endogenous exposures, Aged
Abstract

BACKGROUND: Receptor activator of nuclear factor kappa-B (RANK)-signaling is involved in tumor growth and spread in experimental models. Binding of RANK ligand (RANKL) to RANK activates signaling, which is inhibited by osteoprotegerin (OPG). We have previously shown that circulating soluble RANKL (sRANKL) and OPG are associated with breast cancer risk. Here we extend these findings to provide the first data on pre-diagnosis concentrations of sRANKL and OPG and risk of breast cancer-specific and overall mortality after a breast cancer diagnosis. METHODS: Two thousand six pre- and postmenopausal women with incident invasive breast cancer (1620 (81%) with ER+ disease) participating in the European Prospective Investigation into Cancer and Nutrition (EPIC) cohort were followed-up for mortality. Pre-diagnosis concentrations of sRANKL and OPG were quantified in baseline serum samples using an enzyme-linked immunosorbent assay and electrochemiluminescent assay, respectively. Hazard ratios (HRs) and 95% confidence intervals (CIs) for breast cancer-specific and overall mortality were calculated using Cox proportional hazards regression models. RESULTS: Especially in women with ER+ disease, higher circulating OPG concentrations were associated with higher risk of breast cancer-specific (quintile 5 vs 1 HR 1.77 [CI 1.03, 3.04]; ptrend 0.10) and overall mortality (q5 vs 1 HR 1.39 [CI 0.94, 2.05]; ptrend 0.02). sRANKL and the sRANKL/OPG ratio were not associated with mortality following a breast cancer diagnosis. CONCLUSIONS: High pre-diagnosis endogenous concentrations of OPG, the decoy receptor for RANKL, were associated with increased risk of death after a breast cancer diagnosis, especially in those with ER+ disease. These results need to be confirmed in well-characterized patient cohorts.

7. Osteoprotegerin and breast cancer risk by hormone receptor subtype: a nested case-control study in the EPIC cohort

Author

Fortner, Renée T, Sarink, Danja, Schock, Helena, Johnson, Theron, Tjønneland, Anne, Olsen, Anja, Overvad, Kim, Affret, Aurélie, His, Mathilde, Boutron-Ruault, Marie-Christine, Boeing, Heiner, Trichopoulou, Antonia, Naska, Androniki, Orfanos, Philippos, Palli, Domenico, Sieri, Sabina, Mattiello, Amalia, Tumino, Rosario, Ricceri, Fulvio, Bueno-De-Mesquita, H Bas, Peeters, Petra HM, Van Gils, Carla H, Weiderpass, Elisabete, Lund, Eiliv, Quirós, J Ramón, Agudo, Antonio, Sánchez, Maria-José, Chirlaque, María-Dolores, Ardanaz, Eva, Dorronsoro, Miren, Key, Tim, Khaw, Kay-Tee, Rinaldi, Sabina, Dossus, Laure, Gunter, Marc, Merritt, Melissa A, Riboli, Elio, and Kaaks, Rudolf

Subjects
musculoskeletal diseases, Osteoprotegerin, Breast Neoplasms, Middle Aged, Hormone receptor, 3. Good health, Progesterone receptor, Cohort Studies, RANK axis, Breast cancer, Risk Factors, Case-Control Studies, Estrogen receptor, Humans, Female, Prospective Studies
Abstract

BACKGROUND: Circulating osteoprotegerin (OPG), a member of the receptor activator of nuclear factor kappa-B (RANK) axis, may influence breast cancer risk via its role as the decoy receptor for both the RANK ligand (RANKL) and tumor necrosis factor-related apoptosis-inducing ligand (TRAIL). Circulating OPG and breast cancer risk has been examined in only one prior study. METHODS: A case-control study was nested in the European Prospective Investigation into Cancer and Nutrition (EPIC) cohort. A total of 2008 incident invasive breast cancer cases (estrogen receptor (ER)+, n = 1622; ER-, n = 386), matched 1:1 to controls, were included in the analysis. Women were predominantly postmenopausal at blood collection (77%); postmenopausal women included users and non-users of postmenopausal hormone therapy (HT). Serum OPG was quantified with an electrochemiluminescence assay. Relative risks (RRs) and 95% confidence intervals (CIs) were calculated using conditional logistic regression. RESULTS: The associations between OPG and ER+ and ER- breast cancer differed significantly. Higher concentrations of OPG were associated with increased risk of ER- breast cancer (top vs. bottom tertile RR = 1.93 [95% CI 1.24-3.02]; p trend = 0.03). We observed a suggestive inverse association for ER+ disease overall and among women premenopausal at blood collection. Results for ER- disease did not differ by menopausal status at blood collection (p het = 0.97), and we observed no heterogeneity by HT use at blood collection (p het ≥ 0.43) or age at breast cancer diagnosis (p het ≥ 0.30). CONCLUSIONS: This study provides the first prospective data on OPG and breast cancer risk by hormone receptor subtype. High circulating OPG may represent a novel risk factor for ER- breast cancer.

8. Plasma carotenoids, vitamin C, tocopherols, and retinol and the risk of breast cancer in the European Prospective Investigation into Cancer and Nutrition cohort

Author

Carla H. van Gils, Kim Overvad, Martine M. Ros, Veronique M. Klaasen, Antonia Trichopoulou, Emily Sonestedt, Ruth C. Travis, Florence Perquier, Giovanna Masala, Pilar Amiano, Carmen Navarro, Anne Tjønneland, Kay-Tee Khaw, Claire Cadeau, Pagona Lagiou, Elio Riboli, Genevieve Buckland, Salvatore Panico, Vittorio Krogh, Isabelle Romieu, J. Ramón Quirós, Paolo Vineis, Eva Ardanaz, Timothy J. Key, Dimitrios Trichopoulos, Elisabete Weiderpass, H. Bas Bueno-de-Mesquita, Rosario Tumino, Rudolf Kaaks, Paul Brennan, Guri Skeie, María José Sánchez, Marie-Christine Boutron-Ruault, Heiner Boeing, Malin Sund, Eugene Jansen, Eiliv Lund, Ulrika Ericson, Marije F. Bakker, Matthias Johansson, Tilman Kühn, Nicholas J. Wareham, Noémie Travier, Krasimira Aleksandrova, Petra H.M. Peeters, Anja Olsen, Sabina Rinaldi, Bakker, Marije F, Peeters, Petra Hm, Klaasen, Veronique M, Bueno de Mesquita, H. Ba, Jansen, Eugene Hjm, Ros, Martine M, Travier, Noémie, Olsen, Anja, Tjønneland, Anne, Overvad, Kim, Rinaldi, Sabina, Romieu, Isabelle, Brennan, Paul, Boutron Ruault, Marie Christine, Perquier, Florence, Cadeau, Claire, Boeing, Heiner, Aleksandrova, Krasimira, Kaaks, Rudolf, Kühn, Tilman, Trichopoulou, Antonia, Lagiou, Pagona, Trichopoulos, Dimitrio, Vineis, Paolo, Krogh, Vittorio, Panico, Salvatore, Masala, Giovanna, Tumino, Rosario, Weiderpass, Elisabete, Skeie, Guri, Lund, Eiliv, Quirós, J. Ramón, Ardanaz, Eva, Navarro, Carmen, Amiano, Pilar, Sánchez, María José, Buckland, Genevieve, Ericson, Ulrika, Sonestedt, Emily, Johansson, Matthia, Sund, Malin, Travis, Ruth C, Key, Timothy J, Khaw, Kay Tee, Wareham, Nick, Riboli, Elio, and van Gils, Carla H.

Subjects
0301 basic medicine, antioxidant, medicine.medical_treatment, Medicine (miscellaneous), Physiology, Tocopherols, Ascorbic Acid, Antioxidants, Cohort Studies, chemistry.chemical_compound, 0302 clinical medicine, Prospective Studies, Non-U.S. Gov't, Vitamin A, Carotenoid, 2. Zero hunger, chemistry.chemical_classification, Nutrition and Dietetics, Tocopherol, Research Support, Non-U.S. Gov't, Retinol, carotenoids, Middle Aged, beta Carotene, 3. Good health, European Prospective Investigation into Cancer and Nutrition, Neoplasm Proteins, Multicenter Study, Europe, Postmenopause, Receptors, Estrogen, 030220 oncology & carcinogenesis, Cohort, Female, Case-Control Studie, Breast Neoplasm, Human, Adult, Risk, medicine.medical_specialty, Breast Neoplasms, Research Support, Follow-Up Studie, Neoplasm Protein, 03 medical and health sciences, Breast cancer, breast cancer, Journal Article, medicine, Humans, plasma, Gynecology, Vitamin C, business.industry, Vitamin E, medicine.disease, Ascorbic acid, Carotenoids, Diet, Prospective Studie, 030104 developmental biology, chemistry, Premenopause, Case-Control Studies, Cohort Studie, business, EPIC, Follow-Up Studies
Abstract

BACKGROUND: Carotenoids and vitamin C are thought to be associated with reduced cancer risk because of their antioxidative capacity.OBJECTIVE: This study evaluated the associations of plasma carotenoid, retinol, tocopherol, and vitamin C concentrations and risk of breast cancer.DESIGN: In a nested case-control study within the European Prospective Investigation into Cancer and Nutrition cohort, 1502 female incident breast cancer cases were included, with an oversampling of premenopausal (n = 582) and estrogen receptor-negative (ER-) cases (n = 462). Controls (n = 1502) were individually matched to cases by using incidence density sampling. Prediagnostic samples were analyzed for α-carotene, β-carotene, lycopene, lutein, zeaxanthin, β-cryptoxanthin, retinol, α-tocopherol, γ-tocopherol, and vitamin C. Breast cancer risk was computed according to hormone receptor status and age at diagnosis (proxy for menopausal status) by using conditional logistic regression and was further stratified by smoking status, alcohol consumption, and body mass index (BMI). All statistical tests were 2-sided.RESULTS: In quintile 5 compared with quintile 1, α-carotene (OR: 0.61; 95% CI: 0.39, 0.98) and β-carotene (OR: 0.41; 95% CI: 0.26, 0.65) were inversely associated with risk of ER- breast tumors. The other analytes were not statistically associated with ER- breast cancer. For estrogen receptor-positive (ER+) tumors, no statistically significant associations were found. The test for heterogeneity between ER- and ER+ tumors was statistically significant only for β-carotene (P-heterogeneity = 0.03). A higher risk of breast cancer was found for retinol in relation to ER-/progesterone receptor-negative tumors (OR: 2.37; 95% CI: 1.20, 4.67; P-heterogeneity with ER+/progesterone receptor positive = 0.06). We observed no statistically significant interaction between smoking, alcohol, or BMI and all investigated plasma analytes (based on tertile distribution).CONCLUSION: Our results indicate that higher concentrations of plasma β-carotene and α-carotene are associated with lower breast cancer risk of ER- tumors.

Published
2014
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